CREB − a real culprit in oncogenesis

The cAMP response element‐binding protein (CREB) is a stimulus‐induced transcription factor that responds rapidly to phosphorylation and/or coactivator activation. Regulated activation of CREB has a significant impact on cellular growth, proliferation and survival. To overturn the cellular control o...

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Bibliographic Details
Published in:The FEBS journal 2007-07, Vol.274 (13), p.3224-3232
Main Authors: Siu, Yeung‐Tung, Jin, Dong‐Yan
Format: Article
Language:English
Subjects:
Animals
Cell Proliferation
Cell Survival
Cell Transformation, Neoplastic
CREB
Cyclic AMP Response Element-Binding Protein - metabolism
Cyclic AMP Response Element-Binding Protein - physiology
Dimerization
fusion oncoprotein
Gene Expression Regulation, Leukemic
human T‐cell leukemia virus type I oncoprotein Tax
Humans
Leukemia, Myeloid, Acute - metabolism
Models, Biological
Neoplasms - etiology
Neoplasms - metabolism
oncogenesis
Phosphorylation
Protein Structure, Tertiary
Protein-Serine-Threonine Kinases - metabolism
proto‐oncogene
TORC coactivators
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Summary:The cAMP response element‐binding protein (CREB) is a stimulus‐induced transcription factor that responds rapidly to phosphorylation and/or coactivator activation. Regulated activation of CREB has a significant impact on cellular growth, proliferation and survival. To overturn the cellular control of these processes, tumor cells have developed various mechanisms to achieve constitutive activation of CREB, including gene amplification, chromosome translocation, interaction with viral oncoproteins, and inactivation of tumor suppressor genes. These mechanisms converge on the phosphorylation of CREB and/or the activation of transducer of regulated CREB activity (TORC) coactivators to effect uncontrolled proliferation of cells. This minireview summarizes the different lines of existing evidence that support a direct role of CREB in oncogenesis.
ISSN:1742-464X
1742-4658
DOI:10.1111/j.1742-4658.2007.05884.x